The primary challenge in TB treatment is the emergence of multidrug-resistant TB (MDR-TB). One of the major factors responsible for MDR is the upregulation of efflux pumps. Permeation-glycoprotein (P-gp), an efflux pump, hinders the bioavailability of the administered drugs inside the infected cells. Simultaneously, angiogenesis, the formation of new blood vessels, contributes to drug delivery complexities. TB infection triggers a cascade of events that upregulates the expression of angiogenic factors and P-gp. The combined action of P-gp and angiogenesis foster the emergence of MDR-TB. Understanding these mechanisms is pivotal for developing targeted interventions to overcome MDR in TB. P-gp inhibitors, such as verapamil, and anti-angiogenic drugs, including bevacizumab, have shown improvement in TB drug delivery to granuloma. In this review, we discuss the potential of P-gp inhibitors as an adjunct therapy to shorten TB treatment.
Keyphrases
- mycobacterium tuberculosis
- multidrug resistant
- drug delivery
- drug resistant
- poor prognosis
- gram negative
- cancer therapy
- physical activity
- cell proliferation
- escherichia coli
- stem cells
- acinetobacter baumannii
- pseudomonas aeruginosa
- cystic fibrosis
- klebsiella pneumoniae
- climate change
- vascular endothelial growth factor
- bone marrow